Cross-omics analysis revealed gut microbiome-related metabolic pathways underlying atherosclerosis development after antibiotics treatment.

Objective: The metabolic influence of gut microbiota plays a pivotal role in the pathogenesis of cardiometabolic diseases. Antibiotics affect intestinal bacterial diversity, and long-term usage has been identified as an independent risk factor for atherosclerosis-driven events. The aim of this study was to explore the interaction between gut dysbiosis by antibiotics and metabolic pathways with the impact on atherosclerosis development.

Gut microbiome and cardiometabolic risk.

The last decade has been characterized by an intense research on the composition of the gut microbiome and the links with human health. While previous work was focused on the effects of prebiotics and probiotics, nowadays several laboratories are describing the gut microbiome and its metabolic functions. Gut microbiome interaction with nutrients allows the gut microbiome to survive and at the same time determines the production of metabolites that are either adsorbed by intestinal cell in a mutual relationship or promote detrimental effect.

Posttranslational modulation of FoxO1 contributes to cardiac remodeling in post-ischemic heart failure.

Objective: Forkhead box protein O1 (FoxO1) plays a key role in energy homeostasis, stress response and autophagy and is dysregulated in diabetes and ischemia. We investigated cardiac FoxO1 expression and posttranstranslational modifications after myocardial infarction (MI) and further tested if active posttranstranslational modulation of FoxO1 can alter cardiac remodeling in postischemic heart failure.

Methods: Non-diabetic and diabetic C57BL/6 mice were subjected to MI by ligation of left anterior descending artery.

TIMP3 interplays with apelin to regulate cardiovascular metabolism in hypercholesterolemic mice.

Objective: Tissue inhibitor of metalloproteinase 3 (TIMP3) is an extracellular matrix (ECM) bound protein, which has been shown to be downregulated in human subjects and experimental models with cardiometabolic disorders, including type 2 diabetes mellitus, hypertension and atherosclerosis. The aim of this study was to investigate the effects of TIMP3 on cardiac energy homeostasis during increased metabolic stress conditions.

Methods: ApoE(-/-)TIMP3(-/-) and ApoE(-/-) mice on a C57BL/6 background were subjected to telemetric ECG analysis and experimental myocardial infarction as models of cardiac stress induction.